PROTECTING PERIOPERATIVE VISION
From the American Society of Anesthesiologists’ 2006 Annual Meeting, October 14-18, 2006
| ISCHEMIC EVENTS IN THE POSTERIOR EYE, AND OPTIC NERVE COMPARTMENT SYNDROME —Steven
Roth, MD, Associate Professor and Chief of Neuroanesthesia, Department of Anesthesia and Critical Care, University of
Chicago Pritzker School of Medicine, Chicago, IL
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| Incidence of postoperative visual loss (POVL): 1 in 60,000 in general surgical population (1996 data; subsequently
found to be lower); incidence in spine surgery may be ≤1 in 1000
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| Causes of visual loss: include central retinal artery occlusion (CRAO), ischemic optic neuropathy (ION; posterior
[PION] and anterior [AION]), and cortical blindness
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 | CRAO: almost always due to external compression of eye; emboli and carotid occlusion rare; occurs in perioperative period,
from moving on headrest or improper positioning; animal experiments indicate as little as 20 min before damage
to eye occurs; cascade of events— postischemic hypoperfusion occurs after retinal circulation occluded; results in further
damage, even after occlusion removed; mechanisms of damage include retinal ischemia and anterior chamber ischemia;
extraocular muscles become ischemic, leading to reperfusion, followed by increased swelling; leads to further
increases in compartment pressure in anterior chamber, causing proptosis, damage to extraocular muscles, chemosis
(ie, swelling of conjunctival tissue), and damage to cornea; retina hypoperfused, leading to reperfusion injury and further
retinal cell loss; preventive measures—monitor eyes on horseshoe headrest; if head turned, avoid pressing eye
into headrest; speaker recommends not using headrest, if possible; also avoids use of goggles in prone position (may become
source of compression)
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| ION: AION affects front of eye (visible by fundus examination); PION affects intraorbital portion of optic nerve; proposed
etiologies—hypotension, blood loss, hemodilution, fluids, lengthy surgery, abnormal blood flow (BF) autoregulation
in optic nerve, anatomic variance (eg, low cup-to-disc ratio), use of vasopressors, systemic vascular
disease, hypercoagulable states, and sleep apnea syndrome; other explanations—ION also occurs spontaneously;
common cause of sudden visual loss, independent of surgical procedure; no proof of hypotension and anemia as
causes of vision loss
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| Optic nerve compartment syndrome: large fluid volume resuscitation common in major back cases; significant
number of reports of POVL following radical neck dissection, especially with bilateral ligation of internal jugular
vein (even when staged years apart); facial edema common following spine surgery in prone position (but does not
prove facial edema caused by or even associated with lengthy spine surgery cases in prone position); study in patient
with optic nerve swelling found increased IgE and albumin levels in subarachnoid space, suggesting compartmentalization
and shifting of fluids
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| Relative anatomy and physiology: small branches off ophthalmic artery supply optic nerve; small vessels from posterior
ciliary artery and ophthalmic artery easily compressed; fluid conceivably could build up in optic nerve or be extravasated
out from veins and move into substance of optic nerve; halfway through intraorbital portion of optic nerve, central
retinal vein and central retinal artery (CRA) penetrate into substance of optic nerve; in anterior portion of optic
nerve, branches off posterior ciliary arteries provide supply; posterior portion of optic nerve dependent on penetrating
branches from posterior cerebral artery (PCA) and ophthalmic artery and small branches off CRA
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| Pathophysiology of ION: superior and inferior ophthalmic veins drain into cavernous sinus, pass optic nerve at orbital
apex; possible for venous distention to squeeze optic nerve; increased venous pressure results in decreased perfusion
to optic nerve; increased intracranial pressure also squeezes optic nerve; gravitational force results in pooling of
fluid and, perhaps, increased fluid in and around optic nerve; low cup-to-disc ratio raises suspicion for AION
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| Suspected factors resulting in perioperative ION: lengthy surgery with attendant fluid load; blood loss with decreased
hematocrit; blood loss due to deliberate hypotension or allowing patient to “settle out” at lower blood pressure
(BP); vasopressors used to maintain BP may squeeze optic nerve; positioning head below body; venous pressure increased
in and around optic nerve; low cup-to-disc ratio relevant to AION only (combined to produce decreased O2 delivery)
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| Evidence: no evidence of compartment syndrome fluids seen on magnetic resonance imaging (MRI); no pathologic
studies of fluid compartment syndrome; facial edema common with spine surgery in prone position, yet ION rare; no
case-controlled studies of factors, aside from decreased BP and hemoglobin, and surgery time; addition of colloids
rather than crystalloids may decrease edema
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| Positioning: position high-risk patients (ie, those undergoing lengthy surgery with large blood loss) with head at, or
above, level of heart, and in neutral forward position; keep fluids minimal to maintain perfusion (urine output tends to
decrease in prone position, especially in Wilson frame); monitoring central venous pressure (CVP) questionable; keep
head well supported; check and document head position frequently; minimally invasive spine surgery may, in select
patients, prevent problems
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| Magic bullets (animal studies): nothing currently approved by Food and Drug Administration (FDA); α2 agonists
(eg, dexmedetomidine) may be helpful (based on crush injury studies); erythropoietin also may protect optic nerve; ischemic
preconditioning has resulted in profound neuroprotection in retina
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| Vasopressors and fluids: important to maintain perfusion; patient generally requires fluid resuscitation appropriate
to what occurs at operative site; in select patients (especially hypertensive on angiotensin-converting enzyme [ACE]
inhibitor), fluid resuscitation difficult, may then require vasopressor; use of vasopressor to artificially raise BP (without
first attempting other means of enhancing perfusion) may decrease blood supply in optic nerve
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| Increased risk: no data suggesting cardiovascular disease or advanced age increases susceptibility to POVL; studies
indicate cardiovascular problems occur in relatively healthy patients; tight BP control necessary with poorly controlled
hypertension and evidence of atherosclerosis
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| Discussing risk for visual loss with patient: most clinicians hesitant; logistical problems sometimes occur; surgeon
may be most appropriate person to discuss risk
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| DOES FLUID MATTER ?—John C. Drummond, MD, Professor of Anesthesiology, University of California, San Diego,
School of Medicine, and Staff Anesthesiologist, Veterans Affairs Medical Center, San Diego
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| Spine surgery and POVL: lesions include ION and CRAO; CRAO occurs (vein or artery) because direct pressure
on eye (or perhaps distortion by rotation of orbit) occludes BF to and from retina; no link between fluid administration
and occurrence of CRAO; AION appears to be problem of collateral flow through small vessels and probably perfusion
pressure
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| Fluids: cerebral perfusion pressure defined as mean arterial pressure (MAP; 90-95 mm Hg normal) minus intracranial
pressure; orbital perfusion pressure (OPP; 75 mm Hg normal) defined as MAP minus intraocular pressure (IOP; 15
mm Hg normal); during surgery, not uncommon to lower MAP to 60 to 65 mm Hg (lower limit of autoregulation); one
author found average IOP at end of surgery 40 mm Hg in prone position; turning patient on his or her back resulted in
>15-mm Hg increase in IOP; other authors have validated findings; some suggest fluids administered by anesthesia
provider “are in some way responsible”; when administering common isotonic crystalloids (eg, lactated Ringer’s solution,
normal saline), small molecules and water equilibrate freely across entire interstitial space; but when administering
isotonic colloids (eg, albumin, hetastarch [hydroxyethyl starch; HES]; Hespan), “it is stuck in the compartment
where you put it”; only 20% of isotonic crystalloids remain at equilibrium in vascular tree; 80% enter interstitial space
(inevitably occurs in muscles, orbit, and probably fat); no studies looking at whether space tight enough for expansion
of tissues to result in elevations of IOP (evidence cannot yet confirm existence of phenomenon)
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| Evolving practice: limiting crystalloids and favoring greater use of colloids for maintenance of intravascular volume;
also beginning to consider that third-space allowances historically given to patient probably largely unnecessary; POVL
advisory, at least in terms of summary recommendations, does not address matter of fluid management; no evidence on
which to base recommendation (just theoretic logic); one study shows IOP can be influenced with reasonable amount of
reverse Trendelenburg positioning; advisory states high-risk patient should be positioned so head level with or higher
than heart, when possible; head also should be maintained in neutral forward position; speaker believes panel has made
“thou shalt” recommendation without data to link head position with outcome; advisory also states use of deliberate hypotensive
techniques during spine surgery have not been shown to be associated with development of perioperative visual
loss; no firm suggestion that hypotension might contribute to POVL (but hypotension may be factor in this
phenomenon)
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| Summary: restrict crystalloids until evidence indicates otherwise; carefully support BP until absolutely certain of irrelevance
to POVL
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| AMERICAN SOCIETY OF ANESTHESIOLOGISTS’ (ASA) POVL REGISTRY —Lorri A. Lee, MD, Associate Professor
of Anesthesiology and Neurological Surgery, University of Washington School of Medicine, Seattle
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| Identification of POVL: includes AION (nonarteritic and arteritic [uncommon type]), PION (usually associated
with spine surgery, head-and-neck surgery, and other cases with signs of venous engorgement; almost always nonarteritic),
CRAO, and cortical blindness (usually in cases of profound hypotension or emboli); even neuro-ophthalmologists
have some disagreement about differences between AION and PION in early examination
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| Ophthalmologic diagnoses: peripapillary flame-shaped hemorrhages indicate AION; swelling alone may indicate
PION; on late examination (eg, one week to several months), AION and PION look identical (no swelling or embolic
phenomena); CRAO dramatic and profound funduscopic appearance (white ischemic-looking retina; thin attenuated
vessels; cherry red pathognomonic spot); PION not caused by pressure on globe; low incidence of POVL (1 in 1000 to
1 in 500, even at major spine centers); difficult to study clinically
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| Suggested risk factors for POVL: prone position; venous congestion; prolonged duration; large blood loss with
large fluid shifts; anemia; hypotension; vasopressors; coexisting vascular diseases; intrinsic variability in vascular
anatomy and physiology
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| Cases from POVL registry: collects cases of POVL after nonocular surgery, occurring within ≈2 wk after surgery;
detailed forms available on Internet; anonymous submissions, so no fear of medicolegal retribution (no patient, hospital,
or physician identifiers); 93 spine cases; 87% ION and 11% CRAO (combined AION and PION cases because,
after separate analysis, no significant differences seen in perioperative or patient characteristics)
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| ION: two thirds of 83 spine cases posterior, 23% anterior, and 10% unspecified; patient characteristics—average patient
50 yr of age (range, 16-73 yr); >75% men; 64% ASA physical status I and II; one third ASA physical status III;
younger age does not guarantee immunity; possible protective effect of anatomy or hormones in women; at median
age 50 yr, 41% hypertensive, 16% diabetic, and 46% tobacco users (≥1 of these diseases present in 82% of population);
cannot implicate vasculopathy as risk factor; aspects of surgery—>75% of cases performed in lumbosacral
region; 13% in thoracolumbar region; 6% spanning thoracolumbosacral (TLS) region, and only 5% in cervical region
(short cases with low blood loss); frame also implicated as potential risk factor (30% incidence with Wilson
frame); occurs with all types of headrests (57% with soft foam; 19% in Mayfield pins); number of operative vertebral
levels high (most with ≥4 levels), therefore anesthesia duration lengthy (>94% of cases had ≥6 hr of anesthesia;
≥5 hr in prone position); 82% of ION cases had ≥1 L blood loss; largest group had systolic BP in 80 to 99 mm Hg
range for ≥15 min; in ≈13%, lowest systolic BP ≥100 mm Hg; most 20% to 30% below baseline (40% below baseline
with deliberate hypotension; no studies show reduction in blood loss with deliberate hypotension)
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| CRAO: average age 46 yr; anesthetic duration significantly shorter; less blood loss; lowest hematocrit not significantly
different; no bilateral disease (consistent with head falling to one side and having pressure on one eye); poor
recovery (both groups); Mayfield pins not used; 70% of cases had ipsilateral trauma (eg, bruising, proptosis, periorbital
numbness, and corneal abrasions), suggesting compression of globe on that side; usually results in permanent
complete blindness; no proven beneficial treatment; frequent eye checks should eliminate most cases; horseshoe
headrest should be avoided (difficult to protect eyes)
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| Summary: ION most common lesion; most patients relatively healthy; 94% of patients have anesthetic duration ≥6 hr;
82% have blood loss ≥1 L; etiology of ION unproven; CRAO consistent with globe compression still occurring; most
cases preventable with frequent eye checks
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Educational Objectives
| The goal of this program is to educate the listener about the following topics: ischemic events in the posterior eye, optic
nerve compartment syndrome, fluid issues in vision loss, and the American Society of Anesthesiologists’ (ASA) postoperative
visual loss (POVL) registry. After hearing and assimilating this program, the participant will be better able to:
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| 1. Review the incidence and identify possible etiologies of POVL.
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| 2. Define optic nerve compartment syndrome.
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| 3. Describe the pathophysiology of perioperative ischemic optic neuropathy.
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| 4. Examine the effects of vasopressors and fluids on POVL.
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| 5. Apply various findings from the ASA POVL registry.
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Suggested Reading
Buono LM et al: Perioperative posterior ischemic optic neuropathy: review of the literature. Surv Ophthalmol 50:15,
2005; Chang SH et al: The incidence of vision loss due to perioperative ischemic optic neuropathy associated with
spine surgery: the Johns Hopkins Hospital Experience. Spine 30:1299, 2005; Chung MS et al: Visual loss in one eye
after spinal surgery. Korean J Ophthalmol 20:139, 2006; Deyo RA et al: Spinal-fusion surgery - the case for restraint.
N Engl J Med 350:722, 2004; Gotte K et al: Delayed anterior ischemic optic neuropathy after neck dissection. Arch
Otolaryngol Head Neck Surg 126:220, 2000; Ho VT et al: Ischemic optic neuropathy following spine surgery. J Neurosurg
Anesthesiol 17:38, 2005; Lee LA et al: The American Society of Anesthesiologists Postoperative Visual Loss
Registry: analysis of 93 spine surgery cases with postoperative visual loss. Anesthesiology 105:652, 2006; Miller NR:
New concepts in the diagnosis and management of optic nerve sheath meningioma. J Neuroophthalmol 26:200, 2006;
Myers MA et al: Visual loss as a complication of spine surgery. A review of 37 cases. Spine 22:1325, 1997; Roth S
et al: Postoperative visual loss: still no answers--yet. Anesthesiology 95:575, 2001; Roth S et al: Unexplained visual
loss after lumbar spinal fusion. J Neurosurg Anesthesiol 9:346, 1997; Stevens WR et al: Ophthalmic complications
after spinal surgery. Spine 22:1319, 1997; Warner MA et al: Ulnar neuropathy in medical patients. Anesthesiology
92:613, 2000; Warner MA et al: Ulnar neuropathy in surgical patients. Anesthesiology 90:54, 1999.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue the
faculty reports nothing to disclose.
Drs. Roth, Drummond, and Lee spoke at the American Society of Anesthesiologists’ 2006 Annual Meeting, held October
14-18, 2006, in Chicago, IL. The Audio-Digest Foundation thanks the speakers and the ASA for their cooperation
in the production of this program.
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